PubMed Health⌕ Search

Biomedical subjects

G K Jett

Publications and source records attributed to G K Jett.

At least 19 recordsLinked to original sources
PubMed1992

Calcification of porcine valves: a successful new method of antimineralization.

Despite distinct advantages over mechanical cardiac valve prostheses, the use of bioprosthetic valves remains limited due to poor long-term durability, primarily as a result of tissue calcification. A novel anticalcification process, based on treatment of porcine bioprostheses with a derivative of oleic acid, has been developed by one of us (J.M.G.) (US Patent Number 4,976,733). This process employing 2-aminooleic acid (AOA) was tested in a juvenile sheep model. Terminal studies after a 20-week interval included hemodynamic, radiographic, morphologic, and quantitative tissue calcium analyses. All control valves (n = 4) had thickened, immobile, heavily calcified leaflets, whereas all AOA-treated valves (n = 8) were pliable and free of calcium deposits. Calculated valve orifice areas for controls (0.9 +/- 0.2 cm2) (mean +/- standard error of the mean) was less than for AOA-treated valves (2.0 +/- 0.3 cm2) (p less than 0.05). Radiographic calcification scores were greatly elevated in the control (25.5 +/- 5.6) versus AOA-treated valves (0.5 +/- 0.5) (p less than 0.002). In quantitative mineralization studies, the mean calcium content of the control leaflets was 129 +/- 21 milligrams per gram dry weight cusp tissue versus 7.7 +/- 5.8 mg/g for AOA-treated valves (p less than 0.001). Pathologic examination confirmed heavy calcification in the control leaflets, which was essentially absent in the AOA-treated leaflets. However, cuspal hematomas in areas of structural loosening and surface roughening were noted in AOA-treated valves. This anticalcification process dramatically reduced mineralization of porcine valve prostheses in this model.

Animals↗
PubMed1992

Inhibition of human internal mammary artery contractions. An in vitro study of vasodilators.

The internal mammary artery is currently the preferred conduit for myocardial revascularization; however, perioperative vasospasm of the internal mammary artery may limit its use as a bypass graft. The ability of various vasodilators to inhibit internal mammary artery contraction was investigated with the use of discarded segments of human internal mammary artery not used in coronary artery bypass grafting. Ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 degrees C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated by elevating the extracellular potassium concentration to 70 mmol/L or by exposure to a 10 mumol/L concentration of norepinephrine, and inhibition of contraction by vasodilators was measured. The order of potency to inhibit potassium-induced contraction was as follows: nifedipine > verapamil > nitroprusside > papaverine. At maximal effective doses, nifedipine, verapamil, and papaverine almost completely inhibited potassium-induced contraction, whereas nitroprusside inhibited contraction by only 55%. When norepinephrine was used to contract the arteries, a biphasic relaxation curve was seen with nifedipine, but not with other vasodilator drugs. The order of potency to inhibit norepinephrine-induced contraction was as follows: nifedipine > nitroprusside > verapamil > papaverine. Maximal inhibition of norepinephrine contraction by these vasodilators ranged from 68% to 95%. Nitroglycerin, isoproterenol, and adenosine produced little or no inhibition of internal mammary artery contraction caused by potassium or norepinephrine. Although nifedipine was the most potent vasodilator, papaverine produced the greatest maximal inhibition of both potassium- and norepinephrine-induced contraction of human internal mammary artery.

Adenosine↗
PubMed1988

Influence of minoxidil on myocardial hemodynamics, regional blood flow, and morphology in beagle dogs.

Studies were made of the effects of two doses of minoxidil (3 mg/kg), given 24 hours apart, on cardiovascular hemodynamics, regional myocardial blood flow, and cardiac morphology in beagle dogs. Minoxidil caused increases in mean right atrial and left ventricular end-diastolic pressure. Systemic and pulmonary vascular resistance were reduced; cardiac output was increased. Left ventricular stroke work and the systolic pressure time index were unchanged by monoxidil administration. The diastolic pressure time index and ratio of diastolic/systolic pressure time index were decreased by minoxidil. Regional myocardial blood flow, measured with radioactive microspheres, increased in all regions of the heart except to the left ventricular papillary muscles. Minoxidil increased blood flow to left ventricular subendocardial tissue; however, this increase was significantly less than that observed in corresponding areas of subepicardial tissue, thus reducing the subendocardial/subepicardial tissue blood flow ratio. These results suggest that minoxidil is an effective peripheral vasodilator but may result in inadequate subendocardial perfusion. Morphologic studies disclosed two types of minoxidil-induced cardiac lesions: left ventricular papillary muscle necroses, and hemorrhagic lesions which were most prominent in right atrium and were associated with inflammation, intramural hemorrhage, and fibrinoid necrosis of small arteries. The papillary muscle necrosis were attributed to hypoxia. The atrial lesions were not of ischemic or hypoxic origin, because minoxidil did not decrease blood flow to atrial tissue. It is suggested that the atrial lesions are related to excessive vasodilation.

Animals↗
PubMed1988

Vasodilator drug effects on internal mammary artery and saphenous vein grafts.

The internal mammary artery is a dynamic conduit used for myocardial revascularization in which potential exists for spasm as well as for vasodilation. This study investigated vasodilator drug effects on the mammary artery using nitroprusside and nitroglycerin in vitro to measure the inhibition of contraction of human internal mammary artery and in vivo to examine blood flow through a canine mammary artery. In the in vitro study, ring segments of human internal mammary arteries were suspended on strain gauges in muscle baths containing 37 degrees C Krebs solution for measurement of isometric tension in vitro. Arterial contraction was stimulated with 70 mM potassium and 10 microM norepinephrine, and inhibition of contraction by vasodilators was measured. Nitroprusside was more potent and effective than was nitroglycerin in inhibiting potassium and norepinephrine contraction. The in vivo study utilized a canine (n = 8) right heart bypass preparation that allowed precise control of cardiac output, blood pressure and heart rate, which were maintained constant. The internal mammary artery graft and the saphenous vein graft perfused the same coronary artery bed. Electromagnetic flow probes measured graft flow (with the other graft occluded) before and after 15 min of drug infusion (1 microgram/kg per min). Nitroglycerin significantly increased mammary artery flow 36 +/- 13%, whereas nitroprusside significantly decreased it 12 +/- 2%. Saphenous vein grafts responded differently; graft blood flow decreased with nitroglycerin and increased with nitroprusside. Thus, although nitroprusside was more effective than nitroglycerin in inhibiting mammary artery contraction in vitro, it decreased internal mammary artery graft flow measured in vivo. Nitroglycerin had the opposite effect, increasing mammary graft flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Vasoactive drug effects on blood flow in internal mammary artery and saphenous vein grafts.

The internal mammary artery is a dynamic coronary graft, whereas the saphenous vein graft is passive. Therefore, potential exists not only for beneficial vasodilation but also for catastrophic spasm of the artery. The purpose of this study was to examine blood flow in the internal mammary and saphenous vein grafts during infusion of drugs that are commonly used after cardiac operations. A canine right heart bypass preparation allowed precise control of cardiac output, blood pressure, and heart rate, which were maintained constant during drug infusion. Both the internal mammary and saphenous vein grafts were constructed so that they perfused the same coronary bed: They were anastomosed in a Y fashion to a ligated anterior descending coronary artery. Electromagnetic flow probes measured graft flow (with the other graft occluded) before and after 15 minutes of drug infusion. The order of drug infusion was randomized and changes were compared by tests for paired differences. Phenylephrine (2 micrograms/kg/min) decreased flow in both the internal mammary and saphenous vein grafts, whereas norepinephrine (0.1 microgram/kg/min) increased flow in both grafts. Epinephrine (0.05 microgram/kg/min) increased mammary artery flow 16% +/- 6% but decreased saphenous vein graft flow 9% +/- 7%. Nitroglycerin (1 microgram/kg/min) significantly increased internal mammary flow (36% +/- 13%), from 47 +/- 7 to 59 +/- 7 ml/min (p less than 0.01), whereas flow decreased significantly in the saphenous vein graft 14% +/- 3%, from 64 +/- 9 to 59 +/- 8 ml/min (p less than 0.01). Nitroprusside (1 microgram/kg/min) decreased mammary artery flow 12% +/- 2%, from 50 +/- 7 to 44 +/- 7 ml/min (p less than 0.01), but increased saphenous vein graft flow 25% +/- 8%, from 64 +/- 9 to 77 +/- 7 ml/min (p less than 0.01). All hemodynamic variables were unchanged, except for norepinephrine, which significantly increased the first derivative of left ventricular pressure. The results suggest that flow through the canine internal mammary artery is changed by the drugs commonly used in perioperative management. Epinephrine and nitroglycerin increased internal mammary artery flow and decreased saphenous vein graft flow, whereas nitroprusside had the opposite effect. The vascular reactivity of the internal mammary artery must be considered when these drugs are used after coronary revascularization.

Animals↗
PubMed1987

Circulatory support for right ventricular dysfunction.

New modes of circulatory support for right ventricular dysfunction have recently been described. The present study compared the effectiveness of pulmonary artery balloon counterpulsation with a right ventricular assist device for support of surgically induced right ventricular dysfunction. Right ventricular hypertrophy was created in 16 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy and maintaining the pulmonary artery band. Four unassisted animals developed severe acute right heart failure and died. Six sheep had pulmonary artery balloon counterpulsation with a Dacron graft anastomosed to the proximal pulmonary artery as a reservoir for a 40 ml intra-aortic balloon after the onset of heart failure. The remaining six sheep had a pneumatically activated ventricular assist device inserted between the proximal pulmonary artery and the right ventricular apex. Periods of circulatory support with the balloon pump and the assist device on and off were compared. Decreases in right atrial pressure were observed with both balloon counterpulsation and right ventricular assistance: 14 +/- 1 to 11 +/- 1 mm Hg, p less than 0.0001, versus 19 +/- 2 to 12 +/- 2 mm Hg, p less than 0.0002, respectively. Cardiac output increased with both balloon counterpulsation and ventricular assistance: 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min, p less than 0.001, versus 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min, p less than 0.0002, respectively. Aortic systolic pressure increased in both support groups: 78 +/- 7 to 99 +/- 6 mm Hg, p less than 0.0004, versus 53 +/- 9 to 85 +/- 9 mm Hg, p less than 0.0001, respectively. Ventricular assistance produced greater changes in the right atrial pressure (39% +/- 6% versus 17% +/- 3%, p less than 0.01), cardiac output (153% +/- 39% versus 54% +/- 11%, p less than 0.05), and aortic systolic pressure (85% +/- 13% versus 39% +/- 9%, p less than 0.01). The insertion of a right ventricular assist device caused a significant increment in right ventricular dysfunction. These data, obtained with the devices in place but not operating, showed significantly increased right atrial and right ventricular end-diastolic pressures and approximately 50% less cardiac output than with the pulmonary artery balloon counterpulsation system. The results demonstrate that both modes of circulatory support were effective in reversing surgically induced right ventricular failure.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Left ventricular outflow tract obstruction following mitral valve replacement: effect of strut height and orientation.

The influence of strut position and strut height of Ionescu-Shiley bovine pericardial valves on the degree of left ventricular outflow tract (LVOT) obstruction was studied following mitral valve replacement (MVR) in hypertrophied left ventricles. Left ventricular hypertrophy was created in 6 lambs by constrictive banding of the descending thoracic aorta at 2 weeks of age. MVR was accomplished seven months later utilizing cardiopulmonary bypass and hypothermic cardioplegic arrest. Each animal underwent three consecutive valve replacements with 25-mm bovine pericardial valves randomly inserted in each of the following manners: (1) standard-profile valve with orientation of the struts out of the LVOT; (2) standard-profile valve with a strut oriented into the LVOT; and (3) low-strut profile investigational valve with a strut oriented into the LVOT. Gradients across the LVOT were measured after MVR and then following administration of isoproterenol hydrochloride (0.05 micrograms per kilogram of body weight per minute). No gradient was created with the struts oriented out of the LVOT with or without isoproterenol administration. When a strut was oriented into the LVOT without isoproterenol, the gradients were comparable with the standard- and low-profile valves (7 +/- 2 mm Hg versus 6 +/- 4 mm Hg, respectively). With isoproterenol, however, a significant difference in gradients between the standard- and low-profile valves (65 +/- 20 mm Hg versus 22 +/- 14 mm Hg, respectively) was observed when a strut was oriented into the LVOT. The results show that LVOT obstruction following MVR was related to the orientation of the strut of the bioprosthetic valve, and this obstruction was diminished with a decreased strut height of the Ionescu-Shiley prosthesis.

Animals↗
PubMed1986

Left ventricular outflow tract obstruction with mitral valve replacement in small ventricular cavities.

The inference that mitral valve replacement (MVR) may produce left ventricular outflow tract (LVOT) obstruction has been made, but no comparative hemodynamic studies with various types of prostheses have been done. The purpose of the present study was to compare the gradients created across the LVOT with MVR in young sheep with small left ventricular cavities. Mitral valve replacement was accomplished using cardiopulmonary bypass and hypothermic cardioplegic arrest. Five animals were used for each of the following valves studied: 25-mm Ionescu-Shiley bovine pericardial valve, 25-mm Hancock porcine aortic valve, 2M-6120 28-mm Starr-Edwards ball-valve prosthesis, 25-mm Björk-Shiley 60-degree flat tilting-disc prosthesis, and 25-mm St. Jude Medical hemidisc valve. Gradients across the LVOT were measured after MVR and then during infusion of isoproterenol hydrochloride (0.05 micrograms/kg/min). Following MVR, only the Starr-Edwards valve produced an LVOT gradient (32 +/- 23 mm Hg). Substantial gradients after MVR were seen, however, with isoproterenol administration with the Ionescu-Shiley (47 +/- 4 mm Hg), Hancock (13 +/- 8 mm Hg), and Starr-Edwards (65 +/- 30 mm Hg) valves but not with the low-profile valves (Björk-Shiley and St. Jude Medical). The results of the present study demonstrate that MVR can produce LVOT obstruction. The greatest degree of obstruction was with the high-profile mechanical and bioprosthetic valves.

Animals↗
PubMed1986

Right ventricular assistance for experimental right ventricular dysfunction.

Right ventricular dysfunction frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. The purpose of the present study was to surgically induce right ventricular dysfunction and then provide circulatory support with a right ventricular assist device. Right ventricular hypertrophy was created in 13 neonatal lambs by pulmonary artery banding. Right ventricular dysfunction was produced in all animals by performing a right ventriculotomy with the animal supported by cardiopulmonary bypass. In four unassisted animals the circulation failed after separation from bypass. Seven experimental animals underwent the insertion of a pneumatically activated ventricular assist device between the proximal pulmonary artery and the right ventricular apex. Periods with the right ventricular assist device on and off in each animal were compared. The right ventricular assist device increased cardiac output from 0.72 +/- 0.15 to 2.24 +/- 0.23 L/min (p less than 0.0002), increased left atrial pressure from 7 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0005), and increased aortic systolic pressure from 53 +/- 9 to 85 +/- 9 mm Hg (p less than 0.0001). Right ventricular assistance significantly reduced the right ventricular end-diastolic pressure from 19 +/- 3 to 12 +/- 1 mm Hg (p less than 0.0001). Pulmonary artery peak pressure distal to the band increased from 27 +/- 3 to 52 +/- 5 mm Hg (p less than 0.0001). The results indicate that right ventricular dysfunction can be produced by a vertical cardiotomy in a hypertrophied right ventricle with persistent outflow tract obstruction. Right ventricular dysfunction can be effectively reversed by a right ventricular assist device, which may prove clinically useful in managing patients with refractory right ventricular failure.

Animals↗
PubMed1984

Anaphylactic reaction associated with sulindac.

Reported is the case of an anaphylactic reaction following sulindac ingestion. A 64-year-old man developed marked shortness of breath following the ingestion of a 200-mg sulindac tablet. On admission he had a palpable blood pressure of 50 mm Hg and diffuse inspiratory and expiratory wheezes on auscultation. He demonstrated marked cardiovascular instability for 24 hours following the adverse reaction. He was treated successfully with a continuous intravenous infusion of epinephrine, a corticosteroid, and an antihistamine. Recovery was complete. This case demonstrates that caution is needed in prescribing sulindac and other nonsteroidal anti-inflammatory drugs.

Anaphylaxis↗
PubMed1983

Pulmonary artery balloon counterpulsation for right ventricular failure. An experimental evaluation.

Right ventricular (RV) failure frequently occurs in patients undergoing correction of congenital cardiac defects, as well as in other clinical settings. RV hypertrophy was created in 10 neonatal lambs by pulmonary artery (PA) banding. Twelve months later RV hypertrophy was present (RV weight/body weight = 2.71 +/- 0.31 gm/kg); RV systolic pressures were elevated (65 +/- 9 mm Hg) and the average gradient across the PA band was 38 +/- 9 mm Hg. RV failure was produced in all animals by performing a right ventriculotomy. Four unassisted (control) animals died shortly after separation from bypass. Six experimental animals underwent pulmonary artery balloon counterpulsation (PABCP). A Dacron graft anastomosed to the proximal PA served as a reservoir for a 40 ml intra-aortic balloon pump system. PABCP effectively reversed RV failure, low cardiac output, and systemic arterial hypotension. Periods with PABCP on and off in each animal were compared. PABCP increased cardiac output from 1.45 +/- 0.16 to 2.03 +/- 0.13 L/min (p less than 0.0001) and increased aortic systolic pressure from 78 +/- 7 to 99 +/- 6 mm Hg (p less than 0.0004). PABCP produced a significant reduction in RV peak systolic pressure from 56 +/- 5 to 41 +/- 3 mm Hg (p less than 0.0001). PA peak pressure distal to the band increased from 31 +/- 2 to 40 +/- 1 mm Hg (p less than 0.0001). Right atrial pressure decreased from 14 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001) with PABCP, and RV end-diastolic pressure fell from 15 +/- 1 to 11 +/- 1 mm Hg (p less than 0.0001). RV stroke work index increased 49% from 0.081 +/- 0.011 to 0.121 +/- 0.017 gm X m/kg/beat (p less than 0.01), and RV systolic pressure time index decreased 38% from 1140 +/- 79 to 710 +/- 65 mm Hg sec/min (p less than 0.0001). Thus PABCP in the presence of RV dysfunction can produce substantial improvement in RV function and in overall cardiac function and may prove clinically useful in managing patients in refractory RV failure.

Animals↗
PubMed1982

Five creatine kinase isoenzymes in serum of a patient with severe heart disease.

Abnormal creatine kinase (CK) isoenzyme patterns were observed in the serum of a 64-year-old woman with severe heart disease. Agarose electrophoresis revealed the presence of all the usual CK isoenzymes (MM, MB, and BB) plus an extra band between MM and MB. Total serum CK activity was within the normal range. Within 2 h after the patient suffered cardiorespiratory arrest, a fifth CK isoenzyme appeared, cathodal to MM. After cardiac valve replacement, the patient's serum showed a high activity of CK, but the isoenzyme pattern showed only MM and, transiently, an MB band. With return of the serum CK activity to normal, the CK isoenzymes pattern also became normal, virtually ruling out genetic variant(s). The abnormal CK isoenzyme patterns might have been the consequence of severe hypoxemia in the patient, thus such patients may represent an ominous prognostic sign. The association of the abnormal pattern upon admission with rapid deterioration of the condition of the patient suggests prompt attention for the prevention of complications.

Alanine Transaminase↗
PubMed1981

Intraaortic balloon counterpulsation: its influence alone and combined with various pharmacological agents on regional myocardial blood flow during experimental acute coronary occlusion.

We investigated the separate and combined effects of pharmacological and intraaortic balloon pump (IABP) support on regional myocardial blood flow in an experimental model of acute myocardial ischemia. Chloralose-anesthetized dogs were ventilated with an oxygen-air mixture, and cardiac output, arterial pressure, and heart rate were held constant. Treatment was begun 20 minutes following permanent ligation of the left anterior descending coronary artery (LAD). We evaluated the following pharmacological interventions: 25% hypertonic mannitol, isosorbide dinitrate, methyl-prednisolone sodium succinate, and propranolol. We measured left ventricular hemodynamics and intramyocardial blood flow by the radioactive microsphere technique prior to treatment and at 15-minute intervals thereafter. Compared with control measurements 20 minutes following LAD ligation, collateral blood flow to ischemic myocardium tended to decrease with no treatment. Treatments with the four pharmacological interventions and with IABP alone produced no significant improvement in collateral blood flow to ischemic myocardium 15 minutes following treatment. In contrast, mannitol, isosorbide dinitrate, and propranolol, each combined with IABP support, produced significant improvements in collateral flow within the same time periods. In nonischemic myocardium, combined pharmacological and IABP treatment did not enhance myocardial blood flow above that obtained with the pharmacological agents alone. The most effective combination of mechanisms for improving the ischemic region's myocardial blood flow appeared to be a reduction of extravascular coronary flow resistance coupled with a simultaneous increase in diastolic arterial pressure.

Animals↗